Pressure ulcers, or PRUs, and perineal dermatitis that often lead to PRUs have affected humans throughout history and addressing the management of these pressure ulcers is now a prominent healthcare issue in the United States and elsewhere in the world. A PRU which is also known as a pressure sore is a lesion that develops on the skin and underlying tissues from the unrelieved pressure that occurs usually over a bony prominence. All skin and body tissues rely on an adequate blood supply for oxygen and nutrients. When these tissues are compressed for an extended period from hours to days, the critical blood supply can be cut off which then leads to development of a PRU. Despite advances in nursing care, surgery, medical procedures and education, pressure ulcers remain to this day to be a major cause of morbidity and mortality. This is particularly true for persons with impaired sensation, advanced age or prolonged immobility. Consequently, more than one million PRUs occur in the United States annually.
The incidence of PRUs among hospitalized patients ranges from a low of 2.7% to 29%. The prevalence among hospitalized patients, however, is somewhat higher coming in at 3.5% to 69%. Critical care unit patients have an increased risk of pressure ulcers with a 33% incidence rate and 41% prevalence rate respectively. Hospital admitted elderly patients receiving non-elective orthopedic procedures, such as hip replacements and or treatment of bone fractures are at even greater risk with a 66% incidence rate.
The rate of PRUs in the nursing home environment is in the range of 2.6% to 24%. The incidence is 25% however among residents of acute care hospitals. Patients with preexisting pressure ulcers have a 26% incidence of secondary PRU formation in the subsequent 6-month period following the first incidence. Interestingly while the rate of PRUs in chronic care hospitals is 10.8%, a full 33% of those admitted to a chronic care hospital already have pressure ulcers.
Thankfully with adequate treatment most PRUs heal within a year. Despite that fact, however, about 60,000 people die each year in the United States alone from complications of PRUs. In fact a person that has developed a PRU has a 4.5 times greater risk of death than a person with the identical risk factors but does not have a PRU. Additionally there can arise a secondary complication, wound related bacteremia (i.e. sepsis), and this factor can further increase the risk of mortality up to 55%.
A significant number of the patients who are elderly and/or immobile and susceptible to PRUs are also incontinent. It is well known in the art that incontinence significantly increases the risk of the development of PRUs. The increased risk stems from the chemical and/or physical effects that residual urine has on the skin. Urine typically is composed of 95% water and 5% organic solutes that are composed of mostly urea ((NH2)2CO) and smaller amounts of related compounds.
When a patient is incontinent and their excreted urine is not drained away from the body the urinary urea undergoes chemical decomposition on the skin forming ammonium hydroxide (NH4OH), an alkaline substance that raises the skin pH which favors bacterial and fungal proliferation common in both perineal dermatitis and PRUs. It is not uncommon for perineal dermatitis to facilitate the development of PRUs by the concomitant friction and shear related skin breakdown that results from this type of dermatitis making pressure sores more likely. Once a person's skin is chemically compromised by the NH4OH the abundant ubiquitous levels of microorganisms often result in prolific fungal and bacterial growth on the skin. Candida albicans is the most common fungal infectious agent in cases of perineal dermatitis and Staphylococcous is the most common bacterial infectious agent in cases of perineal dermatitis. In the event that a pressure sore does develop, Staphylococcous and E-coli infections of the pressure sore are more common as a result of the chemical effects of urine on the skin. These infections are more serious affecting deeper tissues which can lead to sepsis and ultimately death of untreated or otherwise uncontrolled.
Incontinence also produces direct negative physical effects on the skin. The persistent presence of moisture on the surface of the skin that results from incontinence causes a reduction in the exposed skin's hardness and temperature. These changes increase the vulnerability to pressure induced blood flow reduction that often result in a PRU. Frequent washing and drying after incontinence related “accidents” further aggravates the skin with frictional damage and this in turn adversely effects the barrier function of the skin.
The management of incontinence and pressure area care using absorbent pads is the most common method. However, research has concluded that the use of absorbent incontinence pads ultimately has an adverse effect on the pressure redistributing qualities of specialized support surfaces being used to prevent a PRU in the first place. These pads often have ridges that result from the folding of the pad at the time of packaging by the manufacturer. These ridges contribute to the effect of pressure and development of a PRU.
Market studies have been performed to estimate the costs of treatment and the costs for hospitals stays for patients who developed PRUs during hospitalization. These costs are in excess of $16.0 Billion a year. Particularly, the PRUs among the elderly who are institutionalized are one of the most costly of all diseases to treat. PRUs add over $1.5 billion of expenditures and an additional 2.8 million Medicare hospital days per year to the United States healthcare system. Depending on the stage of development the cost of treatment for PRUs can range from $3,000 to $50,000 per pressure ulcer. Often time reconstructive surgery is needed and these costs have been estimated to exceed $30,000 per patient and rising. These costs alone, without even considering the cost of human suffering, demonstrate the importance of preventing pressure ulcers (PRUs) in the first place and of cost effective treatment practices for PRUs were they to develop.
Much of the cost and current treatment modalities are expensive and labor intensive. This is the proximate result of the cause of the PRU in the first instance, that being the lack of mobility of the patient whose own body weight and lack of movement impede or prevent adequate blood flow to the pressure points of the body in contact with a support surface such as a bed. This can lead to ulceration and necrosis and even death.
The current art treatment modalities addressing the many aspects of PRU care usually require a multidisciplinary approach. Members of a PRU care team may include:
A primary care physician who oversees the treatment plan;
A physician specializing in wound care;
Nurses or medical assistants who provide both care and education for managing wounds;
A social worker who helps a person or family access appropriate resources and addresses emotional concerns related to long-term recovery;
A physical therapist who helps with improving mobility;
A dietitian who assesses nutritional needs and recommends an appropriate diet; and
A neurosurgeon, orthopedic surgeon or plastic surgeon, depending on whether surgery is required and what type of surgery is needed.
Clearly bringing these resources together can be impossible at times depending upon the stresses present in the existing care facility or treatment regimen. Too often in a public urban hospital setting, or low income nursing home environment, etc., a patient may not be moved for many hours if not days at times. Without the frequent relief of the pressure and the therapeutic movement of the body parts prone to PRUs there is little likelihood that such a patient will recover or fully heal from a PRU, especially if their lack of mobility persists for any protracted period of time.
It is widely recognized in the art that the first step in treating a PRU at any stage is relieving the pressure that caused it. The main strategies to reduce pressure include the following:
Repositioning. A person with PRUs needs to be repositioned regularly and placed in correct positions. People confined to a wheelchair should on their own change position as much as possible or at least every 15 minutes if they are able. At a minimum a person in a wheel chair should have assistance with changes in position at least every hour. People that are confined to bed should change positions at least every two hours. The use of lifting devices in these situations is often used to avoid friction during the repositioning.Support surfaces. There exists in the art many different types of special mattresses, cushions or pads and beds that can help a person lie in a position that will relieve pressure on an existing sore and/or protect vulnerable skin from damage. Additionally there are variety of foam, air-filled or water-filled devices provide cushion for those sitting in wheelchairs. The type of devices used will depend on a person's condition, body type and mobility.
In order to heal properly PRUs need to be free from damaged, dead or infected tissue. Debridement of these tissues is done with various methods the choice of which depends on the severity of the PRU, the general health condition of the patient and the ultimate goal of treatment. Debridement methods include:
1) Autolytic debridement which uses the body's natural process of producing enzymes that break down dead tissue. Analytic debridement can be enhanced with a wound dressing that keeps the PRU moist and clean;
2) Enzymatic debridement which is the use of topical chemical enzymes and dressings engineered to break down dead tissues found in PRUs;
3) Mechanical debridement which uses one of many methods that physically loosen or abrade and remove wound debris. These may include pressurized irrigation devices, whirlpool baths or other specialized dressings;
4) Surgical debridement which involves the cutting away of dead tissue.
The cleaning and dressing of wounds is also quite critical. The care that promotes healing of the wound includes the following:
1) Cleaning is essential to prevent infection. A stage I wound should be gently washed with water and mild soap, however, any open sores should be cleaned with a saline solution each time the dressing is changed.
2) A dressing promotes healing by keeping a wound moist, creating a barrier against infection and keeping the surrounding skin dry. A variety of dressings are appropriate for PRUs, including films, gauzes, gels, foams and various treated coverings. A combination of these dressings may be used.
Pressure sores that fail to heal may require surgical intervention. The goals of surgery include improving the hygiene and appearance of the sore, preventing or treating infection, reducing fluid loss through the wound, and lowering the risk of cancer. The type of reconstruction that's best in any particular case depends mainly on the location of the wound and whether there's scar tissue from a previous operation. In general, though, most pressure wounds are repaired using a pad of the person's own muscle, skin or other tissue to cover the wound and cushion the affected bone (flap reconstruction).
Alternatively PRUs are being treated with a modicum of success with topical hyperbaric oxygen therapy. Oxygen (O2) and their reactive oxygen species are involved in all stages of wound healing such as: modulating cell migration; adhesion; proliferation; neovascularization; remodeling and apoptosis. It is well known in the art of PRU treatment modalities that O2 is vital in the synthesis of collagen, enhancement of fibroblasts, angiogenesis and leukocyte function. Additionally O2 also has key functions in energy metabolism and in the inhibition of microbial growth. As a consequence, tissue hypoxia, caused by disrupted or compromised vasculature, seems to be a key factor that limits PRU healing. Topical oxygen therapies increase the tissue blood oxygenation (pO2) of superficial wound tissue. Superficial pO2 at 2 mm depth at the center of a wound bed can result in an increase of pO2 from less than 10 mm Hg to 40 min Hg in a matter of only a few minutes. Additionally the penetration of oxygen into the tissue of a PRU with topical wound oxygen (TWO2) devices, such as a topical hyperbaric oxygen therapy device can increase the most crucial angiogenesis related growth factor involved in the healing process, vascular endothelial growth factor (VEGF).
The benefits of hyperbaric oxygen therapy are well known in the art. Hyperbaric oxygen has been used topically to treat pressure sores and skin ulcers. Specially constructed devices equipped with controlled pressure seals and automatic relief valves have been used. Typical hyperbaric oxygen therapy uses a constant pressure of generally around 22 mm. Hg (1.03 atmospheres absolute) maintained inside the chamber where the PRU is located using pure oxygen at a flow-rate of 2 to 8 liters per minute with direct discharge to atmosphere. The topical hyperbaric oxygen therapy results in bacterial growth suppression, enhanced granulation, and formation of epithelial cells. However, the vascularisation of the patient being treated does seem to have a direct impact on the success of the treatment. The more vascular the patient, the more successful the outcome. Topical hyperbaric oxygen treatment is typically tolerated well and overall it shortened patients healing time and was also useful in the preparation for plastic surgery repair if needed.
As outlined above incontinence has a direct negative effect on patient outcomes for those being treated for PRUs. The presence of urine and the byproducts of the breakdown of the urea that are present in the urine exacerbate the PRU creating a situation where it is difficult, if not impossible, to heal the effected area.
Clearly there is a long felt need for a device and method of use that would combine the features necessary to at the same time provide an effective urine disposal means in combination with hyberbaric oxygen therapy and skin surface pressure relief and redistribution. There are no such acceptable prior art devices that combine all these features into a safe any easy device to use. While the existing PRU and perineal dermatitis treatment procedures and devices may fulfill their respective particular objectives and requirements, and are most likely quite functional for their intended purposes, it will be noticed that none of the prior art disclose an apparatus or method of use that combines the most effective PRU and perineal dermatitis treatment modalities into one device. As such, there apparently still exists the need for such device, especially considering the 60,000 annual death toll in the United States alone that result from PRUs.
The current invention addresses all of these issues to provide a technology that provides a much more effective, efficient and user friendly device. In this respect, the present invention disclosed herein substantially corrects these problems and fulfills the need for such a device.